Schizophrenia is a debilitating psychiatric disorder characterized by a combination of negative (blunted affect, withdrawal, anhedonia) and positive (paranoia, hallucinations, delusions) symptoms as well as marked cognitive deficits. While the etiology of schizophrenia is currently unknown, the disease appears to be produced by a complex interaction of biological, environmental, and genetic factors. Atypical antipsychotics form the front line in the treatment of schizophrenia and more recently in bipolar disorder. However, up to 30% of schizophrenic patients are not adequately treated by currently available medication. While there are a number of atypical antipsychotic agents currently available, these agents suffer from a high rate of discontinuation due to either patient and/or physician dissatisfaction with efficacy or safety/tolerability. Atypical antipsychotics possess a pharmacology which is thought to underlie their ability to achieve efficacy at positive symptoms via antagonism at dopamine D2 and serotonin 5-HT2A receptors. These activities produce some efficacy on negative symptoms but also contribute to adverse side effects. These adverse side effects include weight gain/metabolic effects (thought to be associated with antagonism at 5-HT2C and antagonism at histamine H1 receptors), extra-pyramidal effects and prolactin secretion (thought to be associated with antagonism at dopamine D2 receptors), sedation (thought to be associated with antagonism at α1 adrenergic and antagonism at histamine H1 receptors) and cognitive impairment (thought to be associated with antagonism at muscarinic M1 receptors). Accordingly, there is a need in the art for atypical antipsychotic agents with better efficacy on positive symptoms, negative symptoms and/or decreased adverse side effects.